We are analyzing https://link.springer.com/article/10.1007/s00702-010-0422-7.

Title:
Macrophages in Alzheimer’s disease: the blood-borne identity | Journal of Neural Transmission
Description:
Alzheimer’s disease (AD) is a progressive and incurable neurodegenerative disorder clinically characterized by cognitive decline involving loss of memory, reasoning and linguistic ability. The amyloid cascade hypothesis holds that mismetabolism and aggregation of neurotoxic amyloid-β (Aβ) peptides, which are deposited as amyloid plaques, are the central etiological events in AD. Recent evidence from AD mouse models suggests that blood-borne mononuclear phagocytes are capable of infiltrating the brain and restricting β-amyloid plaques, thereby limiting disease progression. These observations raise at least three key questions: (1) what is the cell of origin for macrophages in the AD brain, (2) do blood-borne macrophages impact the pathophysiology of AD and (3) could these enigmatic cells be therapeutically targeted to curb cerebral amyloidosis and thereby slow disease progression? This review begins with a historical perspective of peripheral mononuclear phagocytes in AD, and moves on to critically consider the controversy surrounding their identity as distinct from brain-resident microglia and their potential impact on AD pathology.
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Keywords {🔍}

cells, microglia, article, pubmed, google, scholar, macrophages, brain, peripheral, cas, disease, mononuclear, phagocytes, immune, cns, amyloid, alzheimers, mouse, cerebral, brainresident, model, bloodborne, town, mice, plaques, role, expression, bone, cell, inflammation, clearance, studies, marrowderived, recent, response, innate, beneficial, microglial, populations, bbb, macrophage, plaque, capable, transgenic, deposits, parenchyma, wisniewski, nat, med, rezaizadeh,

Topics {✒️}

macrophage colony-stimulating factor major histocompatibility complex produce beta-amyloid fibrils beta/a4 amyloid fibrils bone marrow-derived cells vicious feed-forward cycle cedars-sinai medical center bone marrow-derived macrophages rezai-zadeh contributed equally article download pdf blood-borne phagocyte recruitment immune-repressed microglia cousins blood-borne immune cells myeloid-specific cd11b promoter pro-aβ phagocytic outcomes blood-borne mononuclear phagocytes blood-borne mononuclear cells general lack mhc-ii lysosomal β-amyloid fibrils blood-borne monocyte progenitors app/ps1 mouse model innate immune responses tgf-β-smad2/3 conventional irradiation/transplantation chimeras parenchymal blood-borne macrophages restricting β-amyloid plaques downstream smad2/3 signaling cd11b+cd11c+ nk cells disease beta-amyloid plaques blood-borne macrophages impact wild-type animals blood-borne monocytic origin blood-borne macrophages present termed cd11b-hsvtk mice anti-inflammatory effector cells human brain-resident microglia head-sparring irradiation resulted brain-infiltrating macrophages resembled schematic representation showing central etiological events �macrophage” ifn-γ production astrocyte foot processes innate immune cells immune cell infiltrates marrow-derived cells cell surface receptors targeting brain-resident microglia privacy choices/manage cookies immunological/molecular marker expression bone marrow reconstitution

Questions {❓}

Are infiltrating macrophages beneficial or detrimental in AD?
Can pro-inflammatory macrophages be beneficial in AD?
For example, which subset(s) of peripheral mononuclear phagocytes are most efficient at clearing cerebral amyloid?
How close the fit?
Licastro F, Pedrini S, Caputo L, Annoni G, Davis LJ, Ferri C, Casadei V, Grimaldi LM (2000) Increased plasma levels of interleukin-1, interleukin-6 and alpha-1-antichymotrypsin in patients with Alzheimer’s disease: peripheral inflammation or signals from the brain?
Neuroinflammation and microglial activation in Alzheimer disease: where do we go from here?
Rezai-Zadeh K, Gate D, Szekely CA, Town T (2009a) Can peripheral leukocytes be used as Alzheimer’s disease biomarkers?
Rezai-Zadeh K, Gate D, Town T (2009b) CNS infiltration of peripheral immune cells: D-Day for neurodegenerative disease?
These observations raise at least three key questions: (1) what is the cell of origin for macrophages in the AD brain, (2) do blood-borne macrophages impact the pathophysiology of AD and (3) could these enigmatic cells be therapeutically targeted to curb cerebral amyloidosis and thereby slow disease progression?
Was there a true disparity between microglia and peripheral macrophages regarding Aβ clearance?
Why target peripheral macrophages rather than brain-resident microglia?
Wisniewski’s early findings prompted an intriguing question: what makes peripheral macrophages more adept than brain-resident microglia at phagocytosing Aβ in vivo?
Wyss-Coray T (2006) Inflammation in Alzheimer disease: driving force, bystander or beneficial response?

Schema {🗺️}

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         headline:Macrophages in Alzheimer’s disease: the blood-borne identity
         description:Alzheimer’s disease (AD) is a progressive and incurable neurodegenerative disorder clinically characterized by cognitive decline involving loss of memory, reasoning and linguistic ability. The amyloid cascade hypothesis holds that mismetabolism and aggregation of neurotoxic amyloid-β (Aβ) peptides, which are deposited as amyloid plaques, are the central etiological events in AD. Recent evidence from AD mouse models suggests that blood-borne mononuclear phagocytes are capable of infiltrating the brain and restricting β-amyloid plaques, thereby limiting disease progression. These observations raise at least three key questions: (1) what is the cell of origin for macrophages in the AD brain, (2) do blood-borne macrophages impact the pathophysiology of AD and (3) could these enigmatic cells be therapeutically targeted to curb cerebral amyloidosis and thereby slow disease progression? This review begins with a historical perspective of peripheral mononuclear phagocytes in AD, and moves on to critically consider the controversy surrounding their identity as distinct from brain-resident microglia and their potential impact on AD pathology.
         datePublished:2010-06-02T00:00:00Z
         dateModified:2010-06-02T00:00:00Z
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            Neurodegeneration
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      headline:Macrophages in Alzheimer’s disease: the blood-borne identity
      description:Alzheimer’s disease (AD) is a progressive and incurable neurodegenerative disorder clinically characterized by cognitive decline involving loss of memory, reasoning and linguistic ability. The amyloid cascade hypothesis holds that mismetabolism and aggregation of neurotoxic amyloid-β (Aβ) peptides, which are deposited as amyloid plaques, are the central etiological events in AD. Recent evidence from AD mouse models suggests that blood-borne mononuclear phagocytes are capable of infiltrating the brain and restricting β-amyloid plaques, thereby limiting disease progression. These observations raise at least three key questions: (1) what is the cell of origin for macrophages in the AD brain, (2) do blood-borne macrophages impact the pathophysiology of AD and (3) could these enigmatic cells be therapeutically targeted to curb cerebral amyloidosis and thereby slow disease progression? This review begins with a historical perspective of peripheral mononuclear phagocytes in AD, and moves on to critically consider the controversy surrounding their identity as distinct from brain-resident microglia and their potential impact on AD pathology.
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         Microglia
         Astrocyte
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         Psychiatry
         Neurosciences
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      name:Department of Neurosurgery, Maxine Dunitz Neurosurgical Institute, Los Angeles, USA
      name:Department of Biomedical Sciences, Regenerative Medicine Institute, Cedars-Sinai Medical Center, Los Angeles, USA
      name:Department of Neurosurgery, Maxine Dunitz Neurosurgical Institute, Los Angeles, USA
      name:Department of Biomedical Sciences, Regenerative Medicine Institute, Cedars-Sinai Medical Center, Los Angeles, USA
      name:Department of Neurosurgery, Maxine Dunitz Neurosurgical Institute, Los Angeles, USA
      name:Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, USA

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